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通过复制犬急性呼酸动物模型，动态观察动脉血和脑脊液（ＣＳＦ）酸碱变量发现，在动脉二氧化碳分压（ＰａＣＯ２）和血浆［ＨＣＯ_３~－］分别升高为３．９９９ｋｐａ和３ｍｍｏｌ／Ｌ时，ＣＳＦ二氧化碳分压（ＰＣＯ２）升高值同血浆相似，而ＣＳＦ（ＨＣＯ_３~－）的改变值在两组之间有显著性差异（Ｐ＜０．０１）。６ｈ时，Ⅰ组（脑室注入乙酰唑胺）ＣＳＦ［ＨＣＯ_３~－］平均升高为２．５ｍｍｏｌ／Ｌ；Ⅱ组（脑室注射等量人工模拟ＣＳＦ）ＣＳＦ［ＨＣＯ_３~－］平均升高为６ｍｍｏｌ／Ｌ。结果说明：急性呼酸时，ＣＳＦＨＣＯ_３~－的形成主要来源于脑ＣＯ２的水化作用，乙酰唑胺能减少ＣＳＦＨＣＯ_３~－的形成。ＨＣＯ_３~－形成过程中产生的Ｈ＋可能部分由脑ＮＨ３缓冲。
By means of replicating animal models of acute bengal acupuncture, dynamic changes of acid-base and acid-base variables of arterial blood and cerebrospinal fluid (CSF) were observed. When arterial carbon dioxide partial pressure (PaCO2) and plasma [HCO_3 ~] increased to 3.999 kPa and 3 mmol / , CSF partial pressure of carbon dioxide (PCO2) increased with the plasma similar, and CSF (HCO_3 ~ -) changes in the two groups were significantly different (P <0.01). At 6h, the average CSF [HCO_3 ~] in group I (acetazolamide injected into the ventricle) increased to 2.5mmol / L, and the mean increase of CSF [HCO_3 ~] in group II (intraventricular injection of artificial simulated CSF) / L. The results showed that when acute acidosis, the formation of CSFHCO 3 ~ - mainly comes from the hydration of cerebral CO2, and acetazolamide can reduce the formation of CSFHCO 3 ~ -. The H + generated in the formation of HCO 3 ~ - may be partially buffered by brain NH 3.